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SFM Quiz 2 > Innate Immunity > Flashcards

Innate Immunity Flashcards

1
Q

barriers against disease

A

skin, mucous, lysozomes, pH, sebum, etc

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2
Q

humoral defense against disease

A

bacteriocidal substances, ROI, complement, APP, transport proteins, coagulation proteins, interferon

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3
Q

cellular defense against immunity

A 
blood cells (neutrophils, eosinophils, basophils, monocytes, NK cells) 
tissue: macrophages, dendritic cells, mast cells
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4
Q

skin and mucous membranes contain

A

sebaceous glands and sebum which inhibit microbe growth with a low pH or with antimicrobial stubastances and cilia

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5
Q

inflammation is triggered by

A

injury or invasion

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6
Q

inflammation functions to

A

protect tissues but causes damage and disease too

normally the damage is repaired, but inflammation can become chronic

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7
Q

inflammatory mediators result from vasoactice mediators such as

A

prostaglandins, leukotrienes and histamine from mast cells

bradykinin from kinin system

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8
Q

microbes/injury trigger tissue/sentinal cells

A

mast cells, macrophages, dendritic cells

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9
Q

signs/systems of inflammation and infection

A

blood supply increases, causes redness and warmth

BV are permeable, so swelling happens

immune cells are recruited and kill pathogens, causing tissue debris

WBC attack and release substances to continue inflammation

inflammatory mediators can cause pain by nerve stimulation

body reacts with chills, fever, muscle aches

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10
Q

innate responses are often sufficient to

A

prevent infection in tissues and blood, but might not be enough to overcome large numbers of microorganisms

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11
Q

fever is caused by

A

TNF, IL1, IL6 from macrophages in response to pathogens

controlled by hypothalamus

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12
Q

innate immune cells can tell

A

self from nonself using PAMPs

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13
Q

PAMPs (on the surface of the pathogen!)

A

pathogen-associated molecular patterns

unique to specific classes of pathogens-molecular patterns

cannot be altered, supressed or hidden from the surface

not structurally similar to self-antigens

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14
Q

PAMPs include

A 
porins 
lipoproteins
lipopolysacharadies
teichoic acid
mannoproteins 
b-glycan 
lipoarabinomannan
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15
Q

PRRs

A

example is mannose receptor

bacteria, fungi, and viruses need a glycan with mannose tails

no human cells have glycans with terminal mannose

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16
Q

PRRs are coded in

A

germ line

undergo non clonal distribution meaning that all cells have receptors with idenitical specificities

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17
Q

Toll like receptros

A

pair with eachother and recognize pathogens

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18
Q

Extracellular TLRs

A 
1
2
4
5
6
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19
Q

intracellular TLRs

A

3
7
8
9

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20
Q

TLRs recognize

A

PAMPs and activate inflammation

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21
Q

endosomal TLRs

A

located in endosomes into which microbes are ingested

respond only to nucleic acids

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22
Q

TLR signals activate

A

transcription factors that stimulate expression of cytokines and other mediators for inflammation

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23
Q

nuclear factro kB

A

NF-KB one of the most important TF activated by TLRs

promotes expression of various cytokines and adhesion molecules (MOST important for inflammation)

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24
Q

Interferon regualtory factors

A

another inportant Tf

stimualtes production of antiviral cytokines IFNa/b

aka type I interferons

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25
Q

bacteria

A 
TLR 1
2
4
5
9
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26
Q

viruses

A

3
7
8
9

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27
Q

Fungi

A

2

6

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28
Q

MyD88

A

adaptor protein

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29
Q

TRIF

A

adaptor protein

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30
Q

IRF

A

a transcription factor

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31
Q

IRAK

A

kinase

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32
Q

TRAF6

A

adaptor protein

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33
Q

TLR4 dependent cell activation

A

TLR4, MD2, CD14 and LPS is assebled on pathogen surface

MyD88 binds TLR4 and activates IRAK4 to p1 TRAF6 leading to activation of IKK

IKKp IxB causing its degradation and release of NFkB to go to nucleus

NFkB activates genes for inflammatory cytokines made in cytoplasm and secreted via ER

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34
Q

Pamps activate complexes called

A

inflamasomes containing NLRs

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35
Q

NLRs act as

A

scaffolding proteins

assemble signaling platforms that trigger activation of NF-kB and MAPK

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36
Q

best NLR is

A

NLRP3

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37
Q

inflammasomes activate

A

protease caspase 2

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38
Q

main function of caspase 1 is to make

A

IL-1B and IL-18 which drive inflammation

these are produced in the inflammasome

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39
Q

DAMPs

A

damage associated molecular patterns

danger molecules released in damaged or dying vells

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40
Q

while PAMPs are from pathogens, DAMPs are from

A

cell/ecm

both trigger similar types of inducers and same types of sensors leading to same mediators

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41
Q

DAMPs released a lot in ___ and little in ___

A

necrosis; apoptosis

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42
Q

DAMPs include

A

HGMB1
uric acid
HSPs

when these are released from a necrotic cells trigger TLR 2, 4 and NLRP 3 which trigger NFkB

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43
Q

loss of self tolerance leads to

A

development of autoimmune diseases

DAMPs play a role in development of the loss of self-antigen recognition

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44
Q

PRR-triggered response: fMet

A

Fmet is part of prokaryotes but not eukaryotes

fMet is typical PAMP

neutrophils and macrophages see fMEt to distinguish self from nonself

formyl peptide receptor PRR (GPCR) involved in chemotaxis

phagocytes bind to bacterial proteins starting with fMet and use them to inititate phagocytosis

45
Q

macrophages respond to

A

danger signals-DAMPs and PAMPs

46
Q

mcarophages regulate exravasation of

A

blood into tissue

47
Q

machrophages degrade by

A

phagocytosis and do tissue repair

48
Q

macrophages play a role in inflammation by

A 
cytokines and chemokines 
ROI
NO 
prostaglandins
defensins
49
Q

macrophages present antigens to

A

effetor t cells

50
Q

macrophages immunomodulate meaning

A

maintain homeostasis in tissue

51
Q

mast cells express receptros for

A

many DAMPs and PAMPs

52
Q

mast cells can amplify or supress

A

innate and acquired immune repsonses

53
Q

mast cells secrete

A

proinflammatory
antiinflammatory
immunosupressive products

54
Q

mast cells are located in areas exposed to

A

external environment

regualte vascular permeability and recruitment of blood cells

can modulate effector cells through release of mediators

55
Q

cytokines

A

small proteins secreted by cells

mediate inflammation, immunity, and hematopoeisis

can be endocrine, paracrin and autocrine

56
Q

cytokines in the innate immunity have two different classes

A

proinflammatory

antiinflammatory

57
Q

chemokines

A

small protein chemoattractants important for traffickin immune cells

58
Q

ANTIINFLAMMATORY CYTOKINES

A 
IL 10 (only true antiinflammatory) 
TGF-B
59
Q

Inflammatory cytokines

A

TNFa
IL 1
IL6
IL8

60
Q

activation of the complement system result in

A

procution of several different polypeptide cleavage fragments involved in functions of inflammation

61
Q

all complement pathway prodcuts lead to

A

C3b which activates C5 which forms the MAC which puts holes in plasma membranes and kills pathogems

62
Q

lipoppolysaccharide is the most

A

potent activator on macrpphages for forming inflammatory mediators

63
Q

classic complement pathway initiation

A

binding of one IgM or two IgG on microbial surface

64
Q

classic complement pathway c1 complex binds to

A

IgM or 2xIgG

becomes activated

65
Q

activated C1 cleaves

A

C2 and C4 (one activated C1 molecule can cleave many C2 and C4 molecules)

makes C4b and C4b
makes C2b and C2a

66
Q

C4 covalently attaches to

A

microbial surfaces

67
Q

C2a binds to the

A

surface attached C4b thus forming

C4bC2a=C3 convertase

68
Q

C3 convertase cleaves

A

Cd3 into C3a and C3b

69
Q

C3b deposits on

A

surface of bacteria

70
Q

surface bound C3b is an

A

opsonin and increases phagocytosis by phagocytic cells

71
Q

C3b can form a complex with

A

C3 convertase to make the C5 convertase (c4bc2a3b)

72
Q

C5 convertase cleaves C5 into

A

C5a and C5b

73
Q

C5b initiates

A

MAC (lytic pathway)

74
Q

C5a is teh

A

anaphylactoxin

75
Q

MAC

A

contains C5b, C6, C7, C8 togeher with many C9

leads to cell lysis

76
Q

APP

A

CRP
mannose binding protien
a-acid glycoprotein
serum amyloid P component

77
Q

CRP and MBP

A

fix complement, opsonize

78
Q

mast cell receptors

A

IgE, Ag
PAMPs
cytokine/chemokine receptors
C3a, C5a complement

temperature/pressure

cell to cell contact

79
Q

mast cell effector molecules

A 
histamine
proteases
serotinin
heparin
cytokines IL4,TNF

prostaglandins
leukotriene
cytokines
chemokines

80
Q

interferon gamma a and b activates

A

macrophages

inteface between innate and adaptive

macrophages express all OTHER cytokines

81
Q

cytokines that produce fever

A

6, 1b, TNF-a

82
Q

IL8

A

chemotactic factor, recruites cells to infection (T, basophils, neutrophils)

83
Q

IL12

A

activates NK cells, induces CD4 T cells into Th1 cells

84
Q

without IL 12, goes toward

A

B cell/immunigloblin

85
Q

IL12 also acts on NK and T cells to make

A

IFNy which activates macrophages

86
Q

IL6 generates

A

APP

87
Q

sicknes behaviour syndrome

A

due to TNF-a, IL1, IL6

88
Q

rolling

A

neutrophils come into contact with endothelial cells of blood capillaries and interact with surface adhesion molecules

89
Q

TNFa, IL1, mast cells and macrophages induce activation of endothelial cells which will increase expression of

A

P selectins and E selectins which will bind to their ligands on neutrophils (4 steps)

90
Q

4 steps of binding neutrophils to selectins

A

tethering: neutrophils slow down and roll on endotheliuam, mediated by ligand binding

tight binding: integrins on neutrophils and ligands on endothelial cells

diapedesis: transmigration through endothelium
chemotaxis: IL8 controls migrations of neutrophols to inflammatory sites of tissues

91
Q

LGA1 and VLA4 are the integrins on the

A

neutrophils and monocytes in a low affinity state

while rolling, chemokine on endothelial cell can bind to receptor neutrophils

this binding activates LFA1 and VLA4 to increase affinity and binding with ICAm and VCAM

92
Q

monocyte rolling

A

similar in steps 1-3 as neutrophils

monoyte chemoattractant protein is the most important chemokine that regualtes migration and infiltration of monocutes

matureation of monocute into macrophage is controlled by cytokine microenvironemnt

93
Q

classically activated macrophages

A

m1

induced by TLR and cytokines especially IFNy and are microbicidal and proinflammatory

94
Q

alternatively activated macrophages

A

M2 indcued by IL4 and IL!3

important in tissue repair and fibrosis

95
Q

oxygen dependent intracellular killing is a byproduct of teh

A

respiratory burst taht accompanies phagocytosis

96
Q

events of the respiratory burst

A

oxygen consumption increased

superoxide anion produced converted to H202 by superoxide dismutase

hydrogen peroxide is broken down by catalase

singlet ocygen made

hydroxyl radicals made

myeloperoxidase (toxic peroxidation)

hypochlorite made (antimicrobial)

97
Q

antiviral innate immune response is mediated by

A

type I interferons (a/B) which block viral replication in teh host cell

NK cells which kill virus infected cells

98
Q

type I IFNs induce expression of proteins that interfere with

A

viral replcaition to limit spread of virus

inteferon regulates PKR wich blocks viral RNA translation

IFNs activate nuclease ribonuclease L to degrade viral RNA

activate NK cells to kill infected cells

99
Q

NK cells recognize ligands

A

on infected cells or cells undergoing other types of stress

NK cells kill infected/stressed cells

NK cell eliminate reservoirs of infection by killing of host cells and releasing intracellular pathogens for phagocytosis

100
Q

NK cells secrete

A

IFNy type II

most powerful activator of macrophages to kill phagocutozed microbes

101
Q

NK cells have activating receptors that are called

A

KIR (killer cell Ig like receptors) that recognize stress molecules like MICA and MICB on surface of abn. cells

trigger PTKs

102
Q

NK cells have inhibiting receptors that recognize

A

inhibitory receptors called class I MHC and activate PTP to inihibit activation (KIR binds to this as well to inhbit)

103
Q

insufficient KIR-MHC I binding occurs then the NK cell will

A

kill the target cell

104
Q

if KIRs bind to the MHC I suffiencently, host cells is

A

not killed

105
Q

NK cells kill infected cells with

A

perforins to make holes

granzymes to activate apoptosis

macrohage to eat dying cells

106
Q

somce cells have resistance to innate defense mechanisms like

A

phagocytic resistance
ROS resistance
complement resistance
anitmicrobial peptide antibiotics resistance

107
Q

T cells need two signals to activate

A

signal one: binding of antigen
signal two: costimulatory molex molecues from APC

extra signals from cytokines

108
Q

innate immunity indirectly controsl

A

ab-mediated responses of adaptove immunity (becasue innate activates B and T’s are needed for B’s which make Ab)

109
Q

linking innate and adaptive

A

PRRs activated and mature APC

APC presented to naive T cells

secreted cytokines assist in the development and maturation of T cells

SFM Quiz 2 (25 decks)

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